• Korean Journal of Fisheries and Aquatic Sciences
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• v.20 no.6
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• pp.569-572
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• 1987

The DNA damage by linoleic acid hydroperoxide (LHPO) was investigated in a DNA-LHPO system at $37^{\circ}C$ to elucidate the DNA damage mechanism by lipid peroxidation products. LHPO shelved a great DNA damage with the increase of its concentrations. DNA was completely damaged in a LHPO-DNA(weight ratio, 2:3) system after incubation for 2 days. The degree of DNA ,damage by LHPO was greated than that of linoleic acid. In the quantitative analysis of DNA damage, the decreasing ratio of DNA content was $60\%$ in $84{\mu}g$ LHPO system incubated for 1 day compared to the control solution marked $30\%$. There were no participation of active oxygens on the DNA damage by LHPO.

• Development and Reproduction
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• v.4 no.2
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• pp.203-213
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• 2000

To investigate the effects of reactive oxygen species (ROS) on capacitation, acrosome reaction in human spermatozoa. Human spermatozoa were incubated with xanthine-xanthine oxidase (X-XO), $H_2O$$_2$, sodium nitroprusside (SNP) or lymphocyte. Otherwise, spermatozoa were incubated under low $O_2$ (5 ％) condition. Chlortetracycline (CTC) staining was conducted to assess capacitation and acrosome reaction. Analysis of lipid peroxidation was done by spectrophotometric determination of malondialdehyde (MDA) production in spermatozoa. $H_2O$$_2$, X-XO, SNP and lymphocyte treatment significantly increased capacitated spermatozoa within 1 h of incubation. There was no significant difference in capacitation between low- and high $O_2$ groups. In the presence of low concentration of $H_2O$$_2$, lipid peroxidation decreased significantly. However, under the high concentration of $H_2O$$_2$, lipid peroxidation significantly increased at the end of incubation compared to control. In the presence of high concentration of lymphocytes, lipid peroxidation significantly increased compared to control at 1hr of incubation. There was no significant difference in lipid peroxidation according to $O_2$ concentration examined. Acrosome reaction (AR) was evaluated by CTC staining after the progesterone challenge. In all ROS groups, AR increased compared to control. The X(100 $\mu$M) - XO (100mIU) system was the most potent to induce AR. Taken together, it suggested positive control of AR by ROS and the positive relationship between the lipid peroxidation and AR. The early onset of capacitation in the presence of ROS suggest that ROS might be a positive regulator of sperm capacitation and hyperactivation.

• Korean Journal of Acupuncture
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• v.22 no.1
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• pp.117-132
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• 2005

Objectives : This study was carried out to determine whether Juglandis Semen herbal acupuncture (JSA) exerts the protective effect against toxic agent-induced live. cell damage. Methods : The cell damage was estimated by measuring lactate dehydrogenase (LDH) release, and lipid peroxidation was estimated by measuring maiondialdehyde (MDA), a product of lipid peroxidation, in rabbit liver slices. Results : When tissues were incubated with 0.5 mM Hg for $10{\sim}120\;min$, LDH release and lipid peroxidation were increased as a function of incubation time, and these effects were significantly prevented by addition of 0.1% JSA. Hg increased LDH release and lipid peroxidation in dose-dependent manner over the range of $0.1{\sim}l\;mM$ concentrations, which were reduced by 0.1% JSA. When tissues were treated with 0.5 mM Hg in the presence of $0.05{\sim}l\;%$ JSA, LDH release and lipid peroxidation induced by Hg were prevented by JSA in a dose-dependent fashion. JSA at 0.5 and 1% prevented completely effects of 0.5 mM Hg. When tissues were treated with 0.5 mM Hg for 60 min, LDH release and lipid peroxidation were increased, which were significantly prevented by addition of 0.1 % JSA. tert-Butyl hydroperoxide (tBHP) increased LDH release and lipid peroxidation, which were significantly reduced by 0.1 % JSA. Such protective effects were similar to those of N,N'-diphenyl-p-phenylenediamine (DPPD), a potent antioxidant. When tissues were treated with 0.5 mM Hg, activities of catalase and glutathione peroxidase were inhibited, and glutathione content was also reduced. Such effects were prevented by JSA, but not by DPPD. JSA prevented Hg-induced morphological changes. Conclusions : These results indicate that JSA exerts the protective effect against liver cell injury induced by toxic agents through antioxidant action, and this effect may be attributed to an increase in activities of endogeous anitoxidant enzymes and GSH content. However, antioxidant effect of JSA is different from that of a well-known potent antioxidant DPPD.

• Korean Journal of Food Science and Technology
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• v.25 no.6
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• pp.614-619
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• 1993

Oxidation mechanisms of methyl linoleate with ${\alpha}-Tocopherol$(TML) were investigated by determining oxidized products using GC-MS during oxidation at $37^{\circ}C$ for 9 days. Oxidized products of TML were found to be methyl octanoate, methyl-8-(2-furyl)-octanoate, 9,13-trans, cis isomer and 9,13-trans, trans isomer. In previous report, oxidation products of methyl linoleate(ML) were methyl-8-(2-furyl)octanoate, 9,13-trans, cis hydroperoxide isomer, 9,13-trans, trans hydroperoxide isomer, and 9-TMSO-12,13-epoxy-10-octadecenoate. In the case of ML, 9-TMSO-12,13-epoxy-l0-octadecenoate was produced instead of methyl octanoate in TML. ${\alpha}-Tocopherol$ quinone, as a major oxidized product of ${\alpha}-Tocopherol$ was formed at the 6th day of oxidation. ${\alpha}-Tocopherol$ quinone was produced rather quickly in lipid media than aqueous media. In oxidation of methyl linoleate, it was shown that the first oxidized product was methyl-9,13-hydroxy-octadecadienoate. As second products, methyl-8-(2-furyl)-octanoate, 9-TMSO-12,13-epoxy-10-octadenoate, and methyl octanoate were oxidized from methyl-9-hydroxy-10-trans, 12-trans-octadecadienoate.

• Nutrition Research and Practice
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• v.4 no.1
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• pp.3-10
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• 2010

This study was performed to investigate the effect of desalinated underground seawater (named as 'magma seawater', MSW) of Jeju Island in Korea on lipid metabolism and antioxidant activity. MSW was collected from underground of Han-Dong in Jeju Island, and freely given to high fat diet (HFD)-fed C57BL/6 mice for 10 weeks. Although there were no significant differences in the body weight changes and plasma lipid levels, hepatic triglyceride levels were significantly lower in the MSW group than in the normal tap water (TW)-drunken control group. Furthermore, the activity of fatty acid synthase (FAS) was significantly decreased and carnitine palmitoyltransferase (CPT) activity was increased in MSW group compared to TW group. Similarly, real-time PCR analysis revealed that mRNA expressions of lipogenic genes were lowered in MSW groups compared to the control group. In a morphometric observation on the liver tissue, accumulation of fats was remarkably reduced in MSW group. Meanwhile, in vitro assay, tree radical scavenging activity measured by using diphenylpicrylhydrazyl (DPPH) was increased in MSW group. The 2'-7'-dichlorofluorescein diacetate (DCF-DA) staining followed with fluorescent microscopy showed a low intensity of fluorescence in MSW-treated HepG2 cells, compared to TW-treated HepG2 cells, which indicated that the production of reactive oxygen species by tert-butyl hydroperoxide (t-BHP) in HepG2 cells was decreased by MSW treatment. The antioxidant effect of MSW on t-BHP-induced oxidative stress in HepG2 cells was supported by the increased activities of intracellular antioxidant enzymes such as catalase and glutathione reductase. From these results, we speculate that MSW has an inhibitory effect on lipogenesis in liver and might play a protective role against cell damage by t-BHP-induced oxidative stress.

• BMB Reports
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• v.42 no.9
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• pp.561-567
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• 2009

Although many plant-derived phenolic compounds display antioxidant effects in biological systems, their mechanism of action remains controversial. In this study, the mechanism by which p-coumaric acid (p-CA) performs its antioxidant action was investigated in bovine aortic endothelial cells under oxidative stress due to high levels of glucose (HG) and arachidonic acid (AA), a free fatty acid. p-CA prevented lipid peroxidation and cell death due to HG+AA without affecting the production of reactive oxygen species. The antioxidant effect of p-CA was not decreased by buthionine-(S,R)-sulfoximine, an inhibitor of cellular GSH synthesis. In contrast, pretreatment with p-CA caused the induction of peroxidases that decomposed t-butyl hydroperoxide in a p-CA-dependent manner. Furthermore, the antioxidant effect of p-CA was significantly mitigated by methimazole, which was shown to inhibit the catalytic activity of 'p-CA peroxidases' in vitro. Therefore, it is suggested that the induction of these previously unidentified 'p-CA peroxidases' is responsible for the antioxidant effect of p-CA.

• Korean Journal of Pharmacognosy
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• v.36 no.1 s.140
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• pp.44-49
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• 2005

The protective effects of the DWP-04 [DDB : selenium yeast: glutathione {31.1 : 6.8 : 62.1 (%, w/w)} against hepatotoxicity by carbon tetrachloride $(CCl_4)$ were studied in rats. The rats were intraperitoneally injected with $CCl_4$ (50% in com oil) at initial dose of 1 ml/kg followed by 0.5 ml/kg 3 times during 1 week. The DWP-04 (50, 100 or 200 mg/kg) or its vehicle was administered everyday before the start of $CCl_4$ injection for two weeks. $CCl_4$ induced hepatocelluar degeneration and necrosis, which led to a great increase in serum aminotransferase, alkaline phosphatase activity and serum lipid levels. It was found by biochemical analysis that $CCl_4$ treatment remarkably increased thiobarbituric acid reactive substances and physphatidylcholine hydroperoxide in hepatic tissues and induced antioxidant enzymes such as catalase and superoxide dismutase (SOD). Liver and serum lipids were significantly lower in rats fed on DWP-04 than in rats induced by $CCl_4$ only-treatment. These results suggested that the DWP-04 could be a promising candidate for the protection of liver injury based on the preventive effects against lipid peroxidation and serum biochemical parameters.

• Journal of Microbiology and Biotechnology
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• v.15 no.4
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• pp.887-890
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• 2005

To evaluate the hepatoprotective activity of lactic acid bacteria, their effects on tert-butylperoxide (t-BHP)-induced hepatotoxicity in mice were measured. When lactic acid bacteria at doses of 0.5 and 2 g (wet weight)/kg were orally administered to mice with t-BHP-induced liver injury, these bacteria significantly inhibited the increase of plasma alanine aminotransferase and aspartate aminotransferase activities by $17-57\%$ and $57-66\%$ of the t-BHP control group, respectively. However, these lactic acid bacteria did not protect cytotoxicity induced by t-BHP against HepG2 cells. The inhibitory effects of these lactic acid bacteria at a dose of 15 g/kg were comparable with that of diphenyl dimethyl bicarboxylate at a dose of 0.2 g/kg, which has been used as a commercial hepatoprotective agent. Among these lactic acid Jacteria, Bifidobacterium longum HY8001 exhibited the most potent hepatoprotective effect. These orally administered lactic acid bacteria inhibited liver lipid peroxidation on t-BHP-induced hepatotoxicity of mice. We suggest that lactic acid bacteria may be an effective agent against liver injury.

• Archives of Pharmacal Research
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• v.27 no.8
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• pp.867-872
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• 2004

Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. Mitochondria are especially important in the oxidative stress as ROS have been found to be constantly generated as an endogen threat. Mitochondrial defense depends mainly on super-oxide dismutase (SOD) and glutathione peroxidase (GPx), whereas microsomal defense depends on catalase (CAT), which is an enzyme abundant in microsomes. SOD removes superoxide anions by converting them to $H_2O$$_2$, which can be rapidly converted to water by CAT and GPx. Also, GPx converts hydroperoxide (ROOH) into oxidized-glutathione (GSSG). Ovariectomized (OVX) rats are used as an oxidative stress model. An ovariectomy increased the levels of MDA, one of the end-products in the lipid peroxidative process, and decreased levels of the antioxidative enzymes； SOD, CAT and GPx. However, Chondroitin sulfate (CS) decreased the levels of MDA, but increased the levels of SOD, CAT and GPx in a dose-depen-dent manner. Moreover, inflammation and cirrhosis of liver tissue in CS- treated rats were sig-nificantly decreased. These results suggest that CS might be a potential candidate as an anti oxidative reagent.

• Korean Journal of Food Science and Technology
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• v.52 no.1
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• pp.46-53
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• 2020

Carrots were deep fat fried with sunflower oil (SO), palm oil (PO), and a blend of palm and sunflower oils (PSO with PO:SO as 2:8 or 4:6) at different temperatures (180 and 190℃) and lengths of time (0.5 to 2.5 min). The quality of deep fat fried carrots was determined by the moisture and fat content, color, conjugated dienoic acid (CDA), hydroperoxide, p-anisidine value, and fatty acid composition. The moisture content of fried carrots decreased with increasing frying time, while the fat content increased. The CDA and p-anisidine values of carrots fried with SO were higher than those fried with PO because of greater unsaturated fatty acids content in SO. PSO was a better choice than SO or PO for deep fat frying carrots in the aspects of oxidative stability and ratio of unsaturated to saturated fatty acids. These results indicate that the quality of deep fat fried carrots depends on the type of oil and frying temperature used, as well as the length of time.